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What do a cancerous tumor and fatty buildup in an artery have in common? Their harmful cells may have the same way of hiding themselves from the immune system, a study out today suggests. In the new work, researchers studying atherosclerosis—the progressive buildup of fat-laden cells into arterial plaque—found a signaling molecule that may prevent dead cells in the arteries from being eaten and disposed of. Blocking that signal, they found, reduces arterial plaque in mice. And because their signal blocker is an antibody already in phase I clinical trials for cancer treatment, they’re hoping to make a quick jump into human testing for cardiovascular disease.

“It’s going to be a new platform of therapy, not just another cholesterol-lowering drug,” says Nicholas Leeper, a vascular biologist at Stanford University in Palo Alto, California, and senior author on the new study.

Although cholesterol contributes to atherosclerosis, the story of the disease’s progression is much more complex. When these fatty deposits damage an artery wall, immune cells flock to the scene—notably macrophages, which gobble up dying and damaged cells all over the body. But when they arrive at the inflamed artery, they fail to perform that cleanup. Soon, dying muscle cells and dying macrophages join a growing plaque on the artery wall. Nestled inside is a “necrotic core,” a graveyard of cells that destabilizes the rest of the plaque and makes it prone to rupture, which can block the artery and cause a heart attack or stroke./.../